In previous studies of clinically stable, non-diabetic adults with cystic fibrosis (CF), we made a unique observation. Although these patients had enhanced peripheral insulin sensitivity, they had hepatic insulin resistance as demonstrated by significantly elevated hepatic glucose production (HGP), both fasting and during insulin infusion. We postulate that increased HGP occurs in CF at the expense of body protein and fat stores, promoting an overall catabolic state. Our objective is to characterize the contributions of carbohydrate, protein and fat metabolism to abnormally elevated HGP in CF. We will use a combination of 13C NMR spectroscopy, stable and radioisotopes to accomplish this objective.